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World J Gastrointest Oncol. Mar 15, 2022; 14(3): 654-663
Published online Mar 15, 2022. doi: 10.4251/wjgo.v14.i3.654
Colorectal cancer carcinogenesis: From bench to bedside
Pedro Currais, Isadora Rosa, Isabel Claro
Pedro Currais, Isadora Rosa, Isabel Claro, Department of Gastroenterology, Instituto Portugues de Oncologia de Lisboa Francisco Gentil, Lisboa 1099-023, Portugal
Author contributions: Rosa I and Currais P reviewed the literature and wrote the manuscript; Claro I critically reviewed the manuscript; all authors approved the final version of the manuscript.
Conflict-of-interest statement: The authors have no relevant conflicts of interest to declare.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Isadora Rosa, PhD, Doctor, Department of Gastroenterology, Instituto Portugues de Oncologia de Lisboa Francisco Gentil, Rua Prof. Lima Basto, Lisboa 1099-023, Portugal. isarosa@ipolisboa.min-saude.pt
Received: September 27, 2021
Peer-review started: September 27, 2021
First decision: December 4, 2021
Revised: December 18, 2021
Accepted: February 20, 2022
Article in press: February 20, 2022
Published online: March 15, 2022
Core Tip

Core Tip: Colorectal cancer (CRC) is a major cause of cancer death worldwide. It is a heterogeneous entity and its molecular and genetic features have clinical implications. Three main carcinogenesis pathways, with some overlapping features, are now known to lead to CRC: Chromosomal instability, microsatellite instability, and the “serrated” pathways. Their features, namely, microsatellite instability status and BRAF or KRAS mutation status, among others, have to be studied to assess familial cancer risk and to make adequate therapy choices. Ongoing research will potentially even enlarge basic science’s importance for clinical practice.